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Results for “Lead Poisoning”

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At least 19 recordsLinked to original sources
PubMed1975

[Chronic lead poisoning: Lead gout with giant tophi on the skin, nephrophathy and porphyrinopathy].

Chronic lead nephtropathy, secondary gout (lead-gout) and porphyrinuria may develop after long lasting professional exposure to lead. A printer with giant tophi on his hands and feet excreted a significantly higher amount of lead after infusion of calcium EDTA in comparison with a normal control person. This result indicates an increased mobilization of lead from skeletal deposits. Furthermore, the laboratory findings showed renal insufficency and porphyrinuria up to 1316 mug/l (elevation of total porphyrins with slight or no elevation of delta-amino-levulic acid and porphobilinogene). The clinical triad nephropathy, secondary gout and porphyrinuria seems to be a variant of chronic lead poisoning.

Aged↗
PubMed1977

Lead poisoning from lead-soldered electric kettles.

Lead poisoning occurred in two infants, causing lead encephalopathy in one but no symptoms in the other. Both infants had been fed a formula prepared with water boiled in a lead-soldered electric kettle. The diagnosis was suggested by dense metaphyseal bands in radiographs, illustrating the importance of careful examination of "routine" radiographs, particularly in asymptomatic infants.

Bone and Bones↗
PubMed1978

Surma and lead poisoning.

Blood lead concentrations were measured in 62 Asian children, of whom 37 had definitely had surma applied to their eyes and 25 were thought not to have done. The mean concentration in those who had not used surma was 0.98 +/- SD 0.42 mumol/1 (20.3 +/- 8.7 microgram/100 ml) compared with 1.65 +/- 0.68 mumol/4 (34.2 +/- 14.1 microgram/100 ml) in those who had. Analysis of 29 different samples of surma showed 23 of them to be composed largely of lead sulphide. We conclude that the use of surma is associated with high blood lead concentrations. In our cases most of it had been obtained abroad, and hence government restrictions might be ineffective in limiting its use: a better method of prevention might be to inform the leaders of Asian communities of the risks.

Asia↗
PubMed1978

2,3-Dimercaptosuccinic acid: a new agent for the treatment of lead poisoning.

Using minimally lead-poisoned rats, we have measured urinary and fecal lead excretion in response to 2,3-dimercaptosuccinic acid (DMS) administered i.p. or p.o. and compared it to that induced by dimercaptopropanol (BAL) (i.p.), EDTA (i.p.), D-penicillamine (p.o. and i.p.) and the combination of BAL and EDTA (i.p.). At doses of 30 mg/kg, parenterally administered DMS was as effective as i.p. BAL and these two drugs were more effective than the other treatment groups. However, p.o. DMS was only 20% less effective and was as effective as i.p. EDTA and the combination of EDTA + BAL i.p. and significantly more effective than D-penicillamine p.o. or i.p. Unlike BAL, most lead excretion in response to DMS was via the urine, undoubtedly reflecting the greater water solubility of DMS. When mice were fed a diet containing both lead and DMS, the drug prevented the accumulation of porphyrins in erythrocytes. Studies with 210Pb indicate that this prophylactic effect is not due to an inhibition of lead absorption but rather to enhanced excretion of lead. The residual tissue distribution of 210 Pb administered simultaneously with DMS was not different form that of 210Pb alone. Since DMS is orally effective and its LD50 is 30 times greater than that of BAL, we expect this compound to be clinically useful in the treatment of lead poisoning.

Animals↗
PubMedDate not supplied

Insecticide poisoning of peafowls and lead poisoning in a cockatoo.

The deaths of peafowls and a cockatoo were respectively traced to insecticide and lead toxicities. The specific insecticide could not be identified but was demonstrated in the liver by use of fruit flies. The liver of the cockatoo contained 7.1 ppm of lead. The source was presumably a plastic feeder painted with a leaded paint.

Animals↗
PubMed1992

Management of childhood lead poisoning: a survey.

Published recommendations (1985) for the management of childhood lead poisoning suggest the use of ethylenediaminetetraacetic acid (EDTA) provocation testing and chelation as the mainstay of treatment for blood lead levels between 25 and 55 micrograms/dL. Since 1985 evidence has accumulated indicating that (1) levels of blood lead less than 25 micrograms/dL are detrimental to cognitive development, (2) EDTA provocation testing may result in potentially harmful shifts in the body lead burden, and (3) oral agents such as penicillamine and 2,3-dimercaptosuccinic acid are effective in reducing elevated lead levels. To determine how this evidence impacts on the management of childhood lead poisoning, the authors surveyed the lead poisoning clinics of pediatric departments in the cities estimated by the United States Public Health Service to have the largest number of children affected by lead poisoning. Thirty (70%) of 43 surveys were completed. Respondents indicated that the lowest blood lead level for which they would use a chelating agent to reduce the lead burden was as follows: 50 micrograms/dL (3%), 45 micrograms/dL (3%), 40 micrograms/dL (13%), 35 micrograms/dL (3%), 30 micrograms/dL (27%), 25 micrograms/dL (47%), and 20 micrograms/dL (3%). For all blood lead levels from 20 through 55 micrograms/dL, EDTA was the most frequently recommended chelating agent (chelation and provocation testing). Fifteen percent of responding lead clinics do not use the provocation test under any circumstances. For a child with a negative EDTA provocation test, the percentage of respondents recommending the use of any chelation therapy ranged from 16% for blood lead levels of 25 through 29 micrograms/dL to 66% for levels of 50 through 55 micrograms/dL.(ABSTRACT TRUNCATED AT 250 WORDS)

Chelating Agents↗
PubMedDate not supplied

Pathogenetic considerations of pica in lead poisoning.

An important factor associated with lead poisoning in children is the habit of eating non-food substances, a condition termed pica. In search for underlying mechanisms involved in the pathogenesis of pica, this investigation presents evidence in support of the hypothesis that in many families failure of normal mother-child interaction, paternal deprivation, culturally dependent maternal oral interests and significant stress factors in the home where abundant lead-containing material is available are etiologically related to the development of pica in lead poisoning. Other factors, which have been thought to be associated with pica, are nutritional deficiencies and maladaptive behavior patterns. A multifocal treatment approach is considered to be most effective.

Child↗
PubMedDate not supplied

An overview of the laboratory diagnosis of lead poisoning.

Four tests for the evaluation of lead poisoning are reviewed from both the clinical and methodological aspects. Whole blood or erythrocyte lead measurements appear to provide the best means of assessing the bodily burden of lead with electrothermal and Delves cup flame atomic absorption spectorphotometric techniques providing accurate and precise results. Urine lead is less reliable as a screening test for lead poisoning but is excellent for monitoring the course of ethylenediamine tetraacetic acid (EDTA) therapy. Atomic absorption methods for urine are made difficult by the variable matrix of urine but satisfactory electrothermal and flame procedures have been described. Erythrocyte delta-aminolevulinic acid dehydratase activity is a very sensitive index of lead exposure,--perhaps too sensitive. Analytical procedures for measuring this enzyme are subject to errors and many complicating factors such as lack of stability of the specimen limit the usefulness of the test. Urine delta-aminolevulinic acid is of questionable value as a screening procedure and also is subject to analytical problems.

Clinical Enzyme Tests↗
PubMed1975

Acute lead poisoning: Five cases resulting from self-injection of lead and opium.

Five cases of acute lead poisoning resulted from the self-injection of lead and opium pills which were crushed, heated and suspended in water. Two of the five patients died of illnesses in which hepatic failure and reversible acute tubular necrosis were prominent features. One of these two had a severe neuropathy, with flaccid quadriplegia and respiratory paralysis. The other three patients had relatively minor symptoms but unequivocal biochemical evidence of lead toxicity. Autopsy changes included hepatic degeneration with inclusion bodies, regenerating renal tubular epithelium and wasting of skeletal muscle. Hepatic lead content was extremely high in one case. Chelation therapy in the other fatal case resulted in a fall in blood lead to within normal limits and a clinical improvement, which was terminated by massive haemorrhage from a ruptured innominate artery.

Acute Disease↗
PubMed1976

[Lysosomal enzyme activity in the serum of rats with experimental lead poisoning].

Examination of the effect of experimental lead poisoning on permeability of lysosomal membranes in albino rats demonstrated activation of lysosomal enzymes (alpha-manosidase and beta-acetylglucosaminidase) in the blood serum as soon as the third day after daily administration of lead acetate (20 mg/kg). Apparently damage of the lysosomal membrane played an important role in the pathogenesis of lead poisoning.

Acetylglucosaminidase↗
PubMed1976

Lead poisoning in dogs at the University of Pennsylvania Veterinary Hospital.

Twenty-seven dogs with lead poisoning were admitted to the University of Pennsylvania Veterinary Hospital from July, 1963, to April, 1975. The major source of the lead was paint. A common history was ingestion of plaster or paint scrapings during room renovation. Most of the dogs were less than 1 year old and had clinical signs referable to the gastrointestinal or the nervous system, or both. The gastrointestinal signs, in order of frequency, were vomiting, anorexia, tender abdomen, diarrhea, and constipation. The neurologic signs, in order of frequency, were hysteria, convulsions, ataxia, blindness, and mydriasis. The finding of many nucleated erythrocytes without severe anemia was nearly pathognomonic for lead poisoning. Of 14 affected dogs subjected to abdominal radiography, 9 had evidence of ingested radiopaque material. A mean blood lead concentration of 18.8 mug/100 ml, with a range of 0 to 50 mug/100 ml, was found for 26 dogs that were hospitalized for problems unrelated to lead poisoning. Of the 27 dogs with lead poisoning, 22 had their blood analyzed for lead. This group had blood lead values ranging from 40 to 530 mug/100 ml. Seven of the affected dogs were monitored throughout their period of treatment with calcium ethylenediaminetetraacetate. The concentration of lead in the blood decreased quickly after the initiation of treatment but leveled off after 2 or 3 days. The initial rapid phase probably corresponded to the removal of weakly bound or extracellular lead, whereas the slow phase probably corresponded to strongly bound or intracellular lead.

Age Factors↗
PubMed1978

Chronic lead poisoning in horses.

Lead acetate was fed to 4 groups of 2 horses each to study chronic lead intoxication. A 5th group of 3 horses was maintained as controls. The leas was fed in capsules, with the minimum dosage of 6.25 mg/kg/day of lead as lead acetate (group I). The dose was increased from group I through group IV in an approximate geometric series, with each group being given about 125% of the dose given the previous group. These doses were given for 105 days, a period designated as phase 1. Since clinical signs were not observed after 105 days, the doses were increased and fed for an additional 190 days (days 106 to 295). This period was designated phase 2. The smallest daily dose in phase 2 was set at about 125% of the largest daily dose in phase 1. The doses in each group was increased by about 125% of that of the previous group, as was done in phase 1. Seven horses died or were euthanatized after 18 to 190 days of phase 2 (123 to 295 days after the 1st dose). One horse in group I did not develop any clinical signs of intoxication. Dose-related responses were unnoticed with doses larger than 15.3 mg/kg/day. All horses given lead had increased blood lead and serum iron concentrations. During phase 2, the hematocrit (erythrocyte volume) and hemoglobin contents were depressed. The lead concentration in kidney, liver, spleen, pancreas, brain, bone, and heart was increased in the treated horses. The dose level required to produce lead intoxication was greater than that reported for cattle and that estimated in epizootiologic studies of horses.

Animals↗
PubMedDate not supplied

[Ultrastructure of the cells of the peripheral blood in experimental lead poisoning].

In rabbits exposed to lead poisoning electron microscopy revealed the presence in reticulocytes and erythrocytes of differently sized vacuoles, an amassment of ferritin granules in the mitochondria along with autophaging vacuoles; leucocytes evidenced turgescence of the mitochondria, up to and including their destruction and emptiness; the blood platelets showed an abundant vacuolization with disordered distribution of the serotonin and glycogen granules. The above changes become most spectacular on the 7-21st day after poisoning and by the 50th day they are encountered but in isolated cells.

Animals↗
PubMedDate not supplied

[Role of the laboratory in the diagnosis and treatment of lead poisoning].

A case of therapeutic lead poisoning in a six-week old child is reported, this aetiology being very common in paediatrics. The role of the laboratory in treatment is described, the latter having involved the addition of disodium calcitetracemate to the peritoneal dialysis fluid.

Aminolevulinic Acid↗
PubMedDate not supplied

[The infraclinical diagnosis of lead poisoning (author's transl)].

Laboratory study of 16 workers handling lead made it possible to define a state of infraclinical lead poisoning. Estimation of alpha-dehydrase and of free erythrocytic protoporphyrins is the most sensitive test for diagnostic purposes. The estimation of erythrocytic pyrimidine 5' Nucleotidase would seem to be of value in the diagnosis of mild lead poisoning. The urinary lead tolerance test confirms the diagnosis and indicates the degree of intoxication. Its repetition make it possible to treat the intoxication.

Erythrocytes↗